There have been recent encouraging results in animal studies with administration of beta-amyloid antibodies to mice in order decrease beta-amyloid. They showed the recovery of acetylcholine release and choline absorption in the hippocampus. The learning capacity was also improved. The results have led to related clinical trials in humans. Continuous reduction of beta-amyloid might be another method of addressing alzheimers. This can be done with proteases such as neprilysin, insulin-degrading enzyme, plasmin, and cathepsin B. The intraventricular injection of the human neprilysin gene expressing viruses into amyloid transgenic mouse models has contributed to a decrease in beta-amyloid aggregation and neuronal degradation in the frontal cortex and hippocampus. According to a report, intraventricular injections of the human neprilysine gene expressing fibroblasts into beta-amyloid aggregation transgenic mouse models have resulted in a considerable decrease of amyloid plaques. These studies have provided the evidence that proteases can be used as beta-amyloid reducing therapeutic agents on account of their function of decomposing beta-amyloid and paved the way for cure-oriented studies that focus on protease-expressing neural stem cells.